ArticleMolecular and cellular biochemistry2026
M1 macrophage exosomes inhibit lung adenocarcinoma growth by up-regulating KLF6 via the reduction of ALKBH5-mediated KLF6 demethylation.
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- The impact of m6A modified cargo conveyed by exosomes on the tumor microenvironment.Discover oncology · 2026Review
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5 authors.
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Abstract
M1 macrophage exosomes (M1-Exos) have been shown to play a significant role in regulating Lung adenocarcinoma (LUAD) progression. Krüppel-Like Factor 6 (KLF6) is a widely expressed nuclear transcriptional regulator involving in various key cellular processes and functions as a tumor suppressor. Here, this study aimed to investigate the role of KLF6 in LUAD and whether M1-Exos function in LUAD by KLF6. Levels of mRNA and protein were detected using qRT-PCR and western blotting. Exosomes were isolated from M1 macrophages and co-cultured with LUAD cell lines for functional analysis. In vitro analyses were conducted using 5-ethynyl-2'-deoxyuridine assay, flow cytometry and transwell assay. The N6-methyladenosine (m6A) modification profile was analyzed using the methylated RNA immunoprecipitation assay and the interaction was determined by RNA Immunoprecipitation assay. The murine model was established for in vivo analysis. M1 macrophage exosomes suppressed LUAD cell proliferation, migration and invasion. Further analyses showed that KLF6 was packaged in M1 macrophage exosomes and could be transferred into LUAD cells. Functionally, the incubation of KLF6-decreased M1 macrophage exosomes led to the enhancement of LUAD cell proliferation, migration and invasion. Mechanistically, alkylation repair homolog protein 5 (ALKBH5), an RNA m6A demethylase, could reduce KLF6 m6A modification and then broke the stabilization of KLF6 and decreased its expression in M1 macrophages and LUAD cells. Importantly, ALKBH5 reversed the anticancer effects of M1-Exo on LUAD cells. Moreover, the inhibition of LUAD tumor growth in vivo mediated by M1-Exo was also impeded by ALKBH5. In conclusion, M1 macrophage exosomes inhibited LUAD growth by reducing ALKBH5-mediated KLF6 demethylation.
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